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- Title
PGE2 activates cementoclastogenesis by cementoblasts via EP4.
- Authors
Oka H; Miyauchi M; Sakamoto K; Moriwaki S; Niida S; Noguchi K; Somerman MJ; Takata T; Oka, H; Miyauchi, M; Sakamoto, K; Moriwaki, S; Niida, S; Noguchi, K; Somerman, M J; Takata, T
- Abstract
Destruction of cementum and alveolar bone is the main causative event for the exfoliation of teeth as a consequence of periodontitis. Prostaglandin E(2) (PGE(2)) and PGE receptor subtypes (EPs) play an important role in modulating osteoblast-mediated osteoclastogenesis; however, no information is available on the role of PGE(2) and EPs in regulating cementoblast-mediated cementoclastogenesis. We hypothesized that the PGE(2)-EPs pathway also regulates cementoblasts' ability to activate cementoclasts. For these studies, OCCM-30 cells (a mouse cementoblast cell line) were exposed to PGE(2) and specific EP agonists. PGE(2) (100 ng/mL) and EP4 agonist (1 microM) up-regulated RANKL and IL-6 mRNA levels, while they down-regulated OPG mRNA expression. The EP4 antagonist (1 microM) eliminated these effects of PGE(2). PGE(2) treatment of co-cultures of OCCM-30 cells with bone marrow cells induced TRAP-positive cells via the EP4 pathway. These findings suggest that PGE(2) promotes cementoblast-mediated cementoclastogenesis by regulating the expression of RANKL and OPG via the EP4 pathway.
- Publication
Journal of Dental Research, 2007, Vol 86, Issue 10, p974
- ISSN
0022-0345
- Publication type
journal article
- DOI
10.1177/154405910708601011